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Specific guide to this web site for:

 1.  Medical School
      in Statistics

 2.  Medical Students

 3.  Science media writers

 4.  High School & College
     Statistic Teachers


1. Harvard led MI study

2. JACC study 

   (J. of Amer. Coll.

3. NEJM cath study

4. Amer. J. of Cardio.
    review of literature


Oat bran study

Pregnancy & Alcohol

Are Geminis really
9. Columbia 'Miracle' Study  

Additional Topics:


Limitations of Meta-Analyses

Large Randomized Clinical Trials

Tale of Two Large

Advocate meta-analyses

Network meta-analyses





An article was published by Dabaghi1, et al, evaluating the effects of low dose aspirin on platelets.  Though the data their experiment generated was valid, their conclusions were erroneous because of an incorrect review of the literature in the article.  Their experimental data showed that a low dose of aspirin (81 mg) completely inhibited the aggregation of platelets when a particular type of stimulus was tested (a thromboxane stimulus which is a particular type of prostaglandin). They incorrectly misinterpreted prior studies as suggesting the results of other more potent stimulators of platelet aggregation such as epinephrine or collagen, which is a component of connective tissue, had similar effects to thromboxane.  

There was one trial they could not explain which was an eloquent study reported in the journal of Prostaglandins by Kastor et al2, which showed that a single low dose aspirin did not fully inhibit platelets when a collagen stimulus was used.  When Robert Roberts, M.D., a distinguished academician and one of the authors of this paper, presented some information shortly after this paper was published, he stated his group thought a single low dose of aspirin completely inhibited platelets.  In response to a question about the prostaglandin study by Kastor, et al2, he said his group thought that the prostaglandin study may have used a faulty platelet aggreganometer (a device that measures platelet aggregation) to explain why that study’s results were different than their understanding of the other trial results.

The Dabaghi paper1 reached erroneous conclusions because of incorrectly reviewing the previously performed studies. Quite appropriately Dabaghi et al1 did state that further investigation was needed before low dose aspirin could be advocated in the use of acute ischemic syndromes because they studied normal patients and not patients with a threatened heart attack. There was the potential though for other individuals to see this paper and not appropriately limit applying this information before further studies were performed.

The review of literature in the Dabaghi article was factually incorrect. All the prior data for platelet aggregation was consistent. A single low dose of aspirin does not give the full effects of aspirin on platelet inhibition even in normal subjects.  The Kastor study in Prostaglandins2 has actually previously generated data on thromboxane precipitated aggregation that  the Dabaghi article reliably recreated.  The review of literature was done incorrectly. Therefore, it was not apparent to Dabaghi et al that while thromboxane platelet aggregation was inhibited by low dose aspirin, a single low dose of aspirin did not reliably inhibit the more intense platelet stimulation that occurred with collagen or epinephrine (epinephrine is an adrenaline-like substance).

1. Effects of Low-Dose Aspirin on In Vitro Platelet Aggregation in the Early Minutes After Ingestion in Normal Subjects.  Dabaghi S, Kamat S, Payne J, Marks G, Roberts R, Schafer A, Kleiman N.   Am J Cardiol 1994; 74:720-733

2  Kuster L, Frolich J. Platelet aggregation and thromboxane release induced by arachidonic acid, collagen, ADP, and platelet-activating factor following low dose acetylsalicylic acid in man. Prostaglandins 1986;32:415-423